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Transactions on micronuclear DNA and implications for immune signaling. 微核DNA研究进展及其对免疫信号的影响。
IF 11 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Trends in Biochemical Sciences
Pub Date : 2025-11-20 DOI: 10.1016/j.tibs.2025.10.007
John Maciejowski, Roger A Greenberg

Nuclear envelope formations on missegregated chromosomes or chromosome fragments produce micronuclei. Although they exist largely in an autonomous state, they maintain aspects of chromosome biology that are found in the major nucleus. Aberrant micronuclear envelope behaviors alter communication with the cytoplasm. Micronuclear envelope rupture exposes entrapped chromosomes to DNA-interacting factors, resulting in DNA damage and massive chromosome shattering. Exposure of micronuclear DNA to innate immune sensors has been proposed to trigger inflammatory cytokine production. Such events can direct tumor microenvironments in response to genotoxic therapies. Understanding the formation, rupture, DNA integrity, and detection of micronuclei by immune sensors will provide insights into human disease and suggest approaches for therapeutic intervention. Here we discuss basic studies on micronuclei stability and transactions that affect their chromosomal DNA content.

错误分离的染色体或染色体片段上形成的核膜产生微核。尽管它们在很大程度上以自主状态存在，但它们维持着在主核中发现的染色体生物学方面。异常的微核膜行为改变了与细胞质的通讯。微核膜破裂使被包裹的染色体暴露于DNA相互作用因子中，导致DNA损伤和大量染色体碎裂。微核DNA暴露于先天免疫传感器已被提出触发炎症细胞因子的产生。这些事件可以指导肿瘤微环境对基因毒性治疗的反应。通过免疫传感器了解微核的形成、破裂、DNA完整性和检测将提供对人类疾病的见解，并为治疗干预提供方法。本文讨论了影响其染色体DNA含量的微核稳定性和交易的基础研究。
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引用次数: 0
Subscription and Copyright Information 订阅及版权资料
IF 11 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Trends in Biochemical Sciences
Pub Date : 2025-11-01 DOI: 10.1016/S0968-0004(25)00256-7
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引用次数: 0
Advisory Board and Contents 咨询委员会及内容
IF 11 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Trends in Biochemical Sciences
Pub Date : 2025-11-01 DOI: 10.1016/S0968-0004(25)00253-1
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引用次数: 0
Mining the gut microbiota for defluorination activity 挖掘肠道微生物群的除氟活性。
IF 11 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Trends in Biochemical Sciences
Pub Date : 2025-11-01 DOI: 10.1016/j.tibs.2025.07.003
Camille V. Goemans
The gut microbiota harbors a vast array of enzymes, many with unknown functions. In a recent study, Probst et al. mined this ecosystem to identify potential defluorinating enzymes. Combining molecular dynamics, alanine scanning, and machine learning, they uncovered molecular features critical for defluorination enzymatic activity in human gut microbes.
肠道菌群中含有大量的酶，其中许多酶的功能未知。在最近的一项研究中，Probst等人挖掘了这个生态系统，以确定潜在的除氟酶。结合分子动力学、丙氨酸扫描和机器学习，他们发现了人类肠道微生物中除氟酶活性的关键分子特征。
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引用次数: 0
Tools for illuminating the cell surface glycoRNA landscape 用于照亮细胞表面glycoRNA景观的工具。
IF 11 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Trends in Biochemical Sciences
Pub Date : 2025-11-01 DOI: 10.1016/j.tibs.2025.06.006
Xinming Zhang , Yingying Zhu , Yuan Ma
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引用次数: 0
Daily standup meeting: enhancing accountability and psychological safety 每日站立会议：强化问责和心理安全感。
IF 11 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Trends in Biochemical Sciences
Pub Date : 2025-11-01 DOI: 10.1016/j.tibs.2025.08.009
Stefania Tocci , Aspen L. Hirsch , Jessica W. Tsai
Research laboratories often struggle to maintain a trusting environment which negatively affects team cohesion. Daily standup meetings provide a means to enhance communication, transparency, and psychological safety. In this article, we highlight the potential benefits of integrating daily standup meetings into your laboratory routine to promote accountability and teamwork.
研究实验室经常努力维持一个信任的环境，这对团队凝聚力产生了负面影响。每天的站立会议提供了一种加强沟通、透明度和心理安全感的手段。在本文中，我们强调了将每日站立会议集成到您的实验室例行程序中以促进责任和团队合作的潜在好处。
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引用次数: 0
A tale of two dimers: lanthanide recognition at biomolecular interfaces 两个二聚体的故事：生物分子界面上的镧系元素识别。
IF 11 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Trends in Biochemical Sciences
Pub Date : 2025-11-01 DOI: 10.1016/j.tibs.2025.08.008
Wyatt B. Larrinaga , Joseph A. Cotruvo Jr.
Owing to minuscule differences in ionic radius and coordination numbers, separation of the lanthanides is technologically critical but rife with chemical and geopolitical challenges. Methylotrophic bacteria have evolved pathways for lanthanide acquisition and intracellular sorting of preferred from non-preferred lanthanides. Characterization of two proteins in this pathway, lanmodulin and landiscernin, has revealed mechanisms by which cells differentiate lanthanides. This review focuses on two modes of protein dimerization mediated by lanthanide ion binding at protein interfaces, which propagate picometer-scale differences in ionic radius to quaternary structure. Characterization of these interfaces has led us to propose a lanthanide trafficking pathway that ensures metalation of lanthanide-dependent enzymes. Finally, we discuss how metal ion-mediated protein dimerization may be applied toward improving industrial-scale lanthanide separations.
由于离子半径和配位数的微小差异，分离镧系元素在技术上至关重要，但充满了化学和地缘政治挑战。甲基营养细菌已经进化出了获取镧系元素和细胞内优选和非优选镧系元素的途径。lanmodulin和lan辨析蛋白这两种蛋白在这一途径中的特性揭示了细胞分化镧系元素的机制。本文综述了蛋白质界面上镧系离子结合介导的两种蛋白质二聚化模式，这两种模式将离子半径的皮米尺度差异传播到四级结构。这些界面的表征使我们提出了一种确保镧系元素依赖酶金属化的镧系元素运输途径。最后，我们讨论了金属离子介导的蛋白质二聚化如何应用于改善工业规模的镧系元素分离。
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引用次数: 0
E3 ubiquitin ligases in signaling, disease, and therapeutics 泛素连接酶在信号、疾病和治疗中的应用。
IF 11 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Trends in Biochemical Sciences
Pub Date : 2025-11-01 DOI: 10.1016/j.tibs.2025.07.009
Pirouz Ebadi , Caleb M. Stratton , Shaun K. Olsen
The ubiquitin–proteasome system (UPS) is a central regulator of protein turnover and signaling, with E3 ubiquitin ligases conferring substrate specificity and chain-type control. Recent advances have revealed new mechanistic classes of E3 ligases and expanded our understanding of their roles in disease, including cancer, neurodegeneration, and immune dysfunction. These insights have fueled the development of targeted protein degradation strategies that harness the UPS to eliminate disease-associated proteins. Approaches such as proteolysis-targeting chimeras (PROTACs), molecular glues, and antibody-based degraders are broadening the druggable proteome. Despite this progress, key challenges remain, including limited E3 ligase diversity, difficulties in degrader delivery, and resistance mechanisms. This review outlines recent advances in E3 ligase biology and therapeutic degradation, emphasizing opportunities to expand and refine UPS-targeted interventions.
泛素-蛋白酶体系统（UPS）是蛋白质周转和信号传导的中心调节器，E3泛素连接酶赋予底物特异性和链型控制。最近的进展揭示了E3连接酶的新机制类别，并扩大了我们对其在疾病中的作用的理解，包括癌症，神经变性和免疫功能障碍。这些见解推动了靶向蛋白质降解策略的发展，利用UPS消除疾病相关蛋白质。诸如靶向蛋白水解嵌合体（PROTACs）、分子胶和基于抗体的降解剂等方法正在拓宽可药物蛋白质组。尽管取得了这些进展，但仍然存在一些关键挑战，包括有限的E3连接酶多样性、降解物递送困难和抗性机制。本文概述了E3连接酶生物学和治疗降解的最新进展，强调了扩展和完善ups靶向干预的机会。
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引用次数: 0
Membranes as targets and modifiers of mutant huntingtin aggregation 膜作为突变型亨廷顿蛋白聚集的靶标和修饰剂。
IF 11 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Trends in Biochemical Sciences
Pub Date : 2025-11-01 DOI: 10.1016/j.tibs.2025.08.005
Justin Legleiter
Huntington’s disease (HD) is a neurodegenerative disorder caused by an expanded CAG repeat in the huntingtin (HTT) gene, resulting in an expanded polyglutamine (polyQ) tract in HTT protein. Expanded polyQ tracts cause mutant HTT (mHTT) to aggregate and accumulate as cellular inclusions. Recent studies highlight the interactions between mHTT and different cellular membranes that contribute to HD pathogenesis. Beyond being targets for mHTT-induced damage, membranes modify mHTT aggregation in a complex manner. This review explores the membrane abnormalities observed in a variety of HD models and the interplay between binding to and subsequent aggregation of mHTT on membranes, with an emphasis on N-terminal mHTT fragments. Understanding mHTT–lipid interactions may provide potential targets for therapeutic intervention that would complement other efforts.
亨廷顿氏病（HD）是一种神经退行性疾病，由亨廷顿蛋白（HTT）基因CAG重复扩增引起，导致HTT蛋白中聚谷氨酰胺（polyQ）通道扩增。扩大的多q束导致突变的HTT （mHTT）聚集并积累为细胞包涵体。最近的研究强调mHTT与不同细胞膜之间的相互作用有助于HD的发病。除了作为mHTT诱导损伤的靶标外，膜还以复杂的方式修饰mHTT聚集。这篇综述探讨了在各种HD模型中观察到的膜异常，以及mHTT在膜上的结合和随后的聚集之间的相互作用，重点是n端mHTT片段。了解mhtt -脂质相互作用可能为治疗干预提供潜在靶点，从而补充其他努力。
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引用次数: 0
Mitochondrial dynamics and pore formation in regulated cell death pathways 线粒体动力学和孔形成调控细胞死亡途径。
IF 11 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Trends in Biochemical Sciences
Pub Date : 2025-11-01 DOI: 10.1016/j.tibs.2025.09.001
Lisa Hohorst , Uris Ros , Ana J. Garcia-Saez
Mitochondria act as central hubs for cell death signaling. During apoptosis and regulated necrosis (pyroptosis, necroptosis, and ferroptosis), mitochondria undergo drastic changes including membrane permeabilization, fragmentation, and loss of membrane potential. However, dissection of the mechanisms underlying these processes is challenging because they involve remodeling of mitochondrial membranes coupled to the assembly of protein complexes whose dynamics are difficult to capture. We discuss progress in our understanding of mitochondrial alterations in cell death and highlight state-of-the-art experimental approaches to study them. We focus on advanced single-molecule and correlative microscopy methods which have recently provided unprecedented details about the dynamics and structure of protein complexes in mitochondria and their impact on membrane organization.
线粒体是细胞死亡信号的中枢。在细胞凋亡和受调控的坏死（焦亡、坏死和铁亡）过程中，线粒体发生剧烈变化，包括膜渗透、断裂和膜电位丧失。然而，解剖这些过程背后的机制是具有挑战性的，因为它们涉及线粒体膜的重塑，以及蛋白质复合物的组装，其动力学难以捕捉。我们讨论了我们对细胞死亡中线粒体改变的理解的进展，并强调了研究它们的最先进的实验方法。我们专注于先进的单分子和相关显微镜方法，这些方法最近提供了线粒体中蛋白质复合物的动力学和结构及其对膜组织的影响的前所未有的细节。
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引用次数: 0
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